Fig. 4

Role of ROS in adaptive immunity. Adaptive immunity in tumors involves the capture, processing, and presentation of antigens by DCs, leading to the activation of effector T cells against specific antigens. This process is linked to ROS in several ways. The release of cancer antigens is regulated by the type of cell death, with autophagy or apoptotic cell death determining the release of cancer antigens. The amount of ROS present during antigen presentation affects its efficacy, with inhibition of ROS significantly reducing antigen uptake by DCs. However, modest ROS levels are required for T cell activation and differentiation. NOX2-derived ROS are involved in CD3/CD28 stimulation-mediated CD8 + T cell activation, and TCR activation promotes T cell activation by inducing ROS production and regulating IL2 and IL4 expression. Activated T cells express chemokines in response to ROS, which facilitate their migration to the tumor site, where they can induce apoptosis by expressing death ligands such as FasL and TRAIL. ROS are also involved in IL-2-dependent IL-2 production, and subsequent TNF, IFN-γ, perforin, and granzyme B production, as TCR signaling is sensitive to ROS